Mutation suppression

Protein synthesis inhibition—prokaryotes Protein synthesis inhibition—eukaryotes Mistranslation on ribosomes Nonsense mutation suppression DNA translation Phenotypic suppression Membrane leakiness Nucleic acid binding/precipitation... 

REVERSE MUTATION Mutation that restores the wild-type phenotype or gene function in a mutant may occur either by restoration of the original DNA sequence (back mutation) or by indirect compensation for the original mutation (suppression). 

Mutants in the UPR pathway, haclA, irelA, and rlgl-100 are inositol auxo-trophs and levels of INOl expression in irelA and haclA cells are reduced compared to wild type strains (Cox et al., 1993, 1997 Nikawa and Yamashita, 1992 Sidrauski et al., 1996). The opilA mutation suppresses the Ino- phenotype and restores INOl expression in irelA and haclA cells (Cox et al., 1997). The UPR is also induced in wild type cells grown in the absence of inositol, leading Cox et al. (1997) to propose that activation of the UPR is involved in the mechanism of INOl activation. 

If the variant is now sensitive, the mutated gene needs to be sequenced to determine whether there has been a back mutation(s) to the original amino acid(s), or whether there has been a complementary mutation suppressing the original one(s). 

By examining some of the over one thousand tumor-causing point mutations of p53 in the light of its structure, we can identify features of p53 that are necessary for tumor suppression. The amino acids most frequently changed in cancer cells are at or near the protein-DNA interface residues that are infrequently mutated, if at all, are in general far from the DNA-binding site. 

Thyroid autonomy appears as a solitary toxic nodule or toxic multinodular goitre. In toxic thyroid, the nodule s synthesis and secretion of thyroid hormones is autonomous from the thyroid-stimulating hormone (TSH), which is produced in the pituitary gland. Accordingly TSH is suppressed and the extranodular thyroid tissue is functionally downregulated. Thyroid autonomy occurs frequently in iodine-deficient countries, whereas it is much less common in iodine-sufficient areas. Constitu-tively activating mutations in the TSH receptor and in the Gs a protein are the major molecular aetiology of toxic thyroid nodules. 

Shi M, Wang RS, Zhang H, Zhu YF, Han B, Zhang Y, Jin LJ, Yang ZJ, Xu YP (2006) Sequential treatment with lamivudine and interferon-alpha monotherapies in hepatitis B e antigennegative Chinese patients and its suppression of lamivudine-resistant mutations, J Antimicrob Chemother 58 1031-1035... 

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